||Human intestine contains a dense and diverse community of microorganisms. Normal intestinal microflora comprises an estimated 400 different bacterial species, including probiotics and pathogens; these microbes collectively referred to as the commensal microflora, have an important role in human nutrition and health. Salmonella is a common pathogen during summer in Taiwan. The symptoms of salmonellosis include acute responses, such as nausea, vomiting, abdominal pain, diarrhea, even death, and chronic inflammatory response, such as lymphoid depletion and necrotizing ileitis in the intestine. |
TGF-β (Transforming growth factor β)-phosphorizates and activates Smad2/3 to increase IκBα (nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor), subsequently reduces inflammatory factors, such as NF-κB (Nuclear Factor-kappa B), TNF-α (tumor necrosis factor α) and IL-8 (interleukin 8) expression. Further, Smad 7 negatively regulates TGF-β signaling pathway to augment inflammation. In this study, probiotics (Lactobacillus acidophilus) and Salmonella, and human intestinal Caco-2 cells were employed to investigate how probiotics attenuates Salmonella-mediated intestinal inflammation. The results showed that Salmonella infection induced maximal NF-κB expression and TNF-α secretion at the concentrations of 107 CFU/ml; however, probiotics-pretreated cells had significantly lower TNF-α and NF-κB than those with Salmonella infection alone (p<0.05). They also had relatively higher activity of TGF-β/Samd3/4 (p<0.05). Moreover, IκBα expression in probiotics-pretreated cells was higher than that of S. typhimurium infection alone, but Smad 7 expression was lower in probiotics-pretreated cells. Consistent with Smad7 expression, miR-21, a down-regulator of Smad 7, was significantly higher in probiotics and synbiotics-pretreated cells compared with that of S. typhimurium infection alone. The experimental results showed that probiotics effectively attenuated Salmonella-induced intestinal inflammation in human intestinal Caco-2 cells via TGF-β1/Smads and TGF-β1/miR21 signaling pathway.